Models of Addiction: Integrating Approaches

Models of Addiction: Integrating Approaches

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By: Duncan Green

Given the recent surge in addiction rates and overdoses, especially concerning opioids, it may be time to reconsider how addiction is viewed and considered by the academic and lay communities. Both groups have different opinions and perceptions on addiction. Given the terminology used regarding the recent opioid crisis—ie “epidemic” among others—the current, most widely believed model is that addiction is a disease. It is thought that excessive prescription of opioids is to blame for this surge in addiction rates. Although addiction can be a nebulous term with a variety of different criteria, it is generally accepted to be a disorder in which an individual demonstrates prolonged problematic use of a substance which negatively impacts their wellbeing and livelihood, as per the National Institute on Drug Abuse (NIDA).1 With the failure of the disease model and the associated “War on Drugs,” we should perhaps move beyond viewing addiction as a disease.

Theoretical modelling of addiction may seem like an issue that is restricted to the academic field, but it directly affects how the public perceives and approaches the problem of addictions. For the past several decades, the prevailing model of addiction adapted by the public is the disease model of addiction, which is largely beyond the control of an individual with a history of relapse. This has also been referred to as the NIDA model, largely due to how closely associated the National Institute is with promoting the concept that drug addiction as a disease.2 Origins of the NIDA model may also be largely attributed to the “War on Drugs” campaign started during the Reagan administration in the United States. Along with the “Just Say No” campaign, this movement was an effort to prevent behaviours of drug use and drug seeking from starting in the first place. After several decades and billions of dollars, it can be concluded that the war on drugs has soundly failed. An excellent example is the increase popularity of oxycontin, a prescription opioid that has made its way into the streets.3

Another model gaining popularity within academic circles is the incentive salience model. This model portrays addiction as a disorder of motivation and cues rather than a disease that is beyond control.4 In brief, individuals with drug addictions see cues that are relevant to their addiction, such as bottles of alcohol, packs of cigarettes, or bags of white powder. These cues activate various neural reward circuits, such as the subcortical reward pathway, and cause the individual to crave the drug. This model addresses a key problem present in the NIDA disease model: addicted individuals are largely self-medicating to ward off the effects of drug withdrawal. This is irrelevant for drugs with low withdrawal effects, such as cocaine and other stimulants, and behavioral addictions, such as gambling and internet use disorders. On a societal level, it forces a false dichotomy on the public perception of addiction. If addiction is not viewed as a disease, the alternative is to regard addiction as a failure of character and self-discipline.

The incentive salience model also accounts for various sociological and environmental factors. It is commonly acknowledged that individuals living in areas with prominent drug use are much more likely to relapse into use.5 It is worth noting that individuals who live in such areas are also at a higher risk of starting drug use. This greater relapse rate may be due to the increase in availability of addiction-relevant cues and stimuli. By increasing the cravings, these cues increase the likelihood for the individual to seek out the drug, using them at higher doses and more frequently. While this model can compensate for areas of weakness in the NIDA model, it also has its flaws. It deemphasizes many of the systemic physiological issues in addicted individuals, such as withdrawal and long-term neural damage. Animal models observing drug dependence in the absence of drug related stimuli by drug perfusion alone also creates issues with the incentive salience model, as there are no stimuli that the animal could use as cues.

Personally, my research examines the neurobiological markers of psychiatric disorders, focusing mostly on addiction and anxiety disorders. Neuroimaging has been a tool used to argue both sides of the modelling argument. Many studies show long term damage to neurochemical systems associated with drug use. This damage is portrayed as analogous to any other disease, beyond the control of the individual. Further studies have shown neural differences in the reaction to stimuli related to drug use, demonstrating differences in activation of the subcortical dopamine system. The subcortical dopamine system is largely involved with reward reinforcement and “feel-good” responses. While these findings are replicable and strong, these findings have also been used to argue entirely opposing theories of addiction. Changes in activation of the dopamine system can be seen as either damage analogous to disease, or as a change in decision making process, thus being applicable to either model.

Although the constant debate and comparisons of validity for different models of addiction seem like a theoretical exercise, there are some very important real-world implications of the models. For example, a model based solely on the assumption of addiction as a disease would potentially bias clinicians towards relying more heavily on medications as a mode of treatment. On the other hand, a model based solely on reactions towards stimuli may bias clinicians to rely more heavily on cognitive and behavioural therapies for treatments while disregarding the significant physiological issues. It is for this reason that it would be best to take an integrated approach to addiction modelling.

Overall, re-examining the fundamental definition of an addiction influences not only the public perception of addiction and individuals with addictions, but also the care that addicted patients receive from clinicians. It is for this reason that we need to take a more holistic and comprehensive approach to addiction in order to accommodate aspects of both the disease model and the incentive salience model of addiction.


  1. NIDA. (2015, July 29). Addiction Science. Retrieved from
  2. topics/addiction-science on 2018, November 19
  3. Hall, W., Carter, A., & Forlini, C. (2015). The brain disease model of addiction: is it supported by the evidence and has it delivered on its promises? The Lancet Psychiatry, 2(1), 105–110.
  4. Manchikanti, L., Helm, S., Fellows, B., Janata, J. W., Pampati, V., Grider, J. S., & Boswell, M. V. (2012). Opioid epidemic in the United States. Pain Physician, 15(3 Suppl), ES9-38. Retrieved from
  5. Huys, Q. J. M., Tobler, P. N., Hasler, G., & Flagel, S. B. (2014). The role of learning-related dopamine signals in addiction vulnerability. In Progress in brain research (Vol. 211, pp. 31–77).